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Physical Signs of Inspection and Medical Eponyms of Pericarditis Part II: 1864 to 1895.


Inspection is the initial step performed during the physical examination. Information obtained through a careful and deliberate observation is unfortunately often overlooked and underappreciated, although important, since it may provide clues about the condition of the patient and the underlying disease process. Physicians from the midto late eighteenth century used their physical examination skills of observation viewing the venous pulses, chest wall, and abdominal movements during the cardiac and respiratory cycle as a method to diagnose pericardial effusion or adhesive pericarditis. Although observation seems like a simple technique, it in fact requires training, patience, perceptibility, and practice. These observations, recognized as medical eponyms, honor those physicians who initially reported these signs. In the second part of the three-part series on inspection of the pericardium, the history of physicians who observed the sign as originally described and the sensitivity, specificity, and predictive value of its application in modern-day clinical practice are summarized. The signs are presented chronologically, based on the year that they were first reported.


PubMed, Medline, online Internet word searches, and bibliographies from the source text and textbooks sources were used. PubMed was searched using the Medical Subject Heading of the name of the eponym and text words associated with the sign.

Friedreich Sign

Nikolaus Friedreich (1825-1882) was born in Wurzburg, Germany, studied medicine in Wurzburg in 1844 and Heidelberg in 1847, and received his doctorate in 1850 (1, 2). In 1853, he habilitated as Privatdozent (adjunct professor) for special pathology and therapeutics and in 1857 was appointed Professor Extraordinarius of Pathologic Anatomy in Wurzberg, a position formerly held by Rudolf Virchow (2, 3). In 1858, Friedreich was appointed Director of the Medical Clinic, Professor and Chair of Pathology and Therapeutics, and Professor Ordinarius at the University of Heidelberg (2). As a student of Rudolf Virchow in Wurzberg, Friedreich was profoundly influenced by his approach to medicine founded on the principles of cellular pathology and pathological process. His area of special interest was in clinical diagnostics. In collaboration with Kekule, Friedreich determined that amyloid (term coined by Virchow) was a proteniaceous substance (2). His name is perhaps best recognized and associated with his work on hereditary spinal ataxia (Friedreich's ataxia), as described in his paper titled "Ueber Ataxie mit besonderer Berucksichtigung der hereditaren Formen" ("About Ataxia With Special Consideration of the Hereditary Forms") published in Virchow's Archives in 1877. As a description of Friedreich's scientific approach:
All the works of Friedreich, however, the smallest as well as the most
extensive, have a common and characteristic character; built on the
firm foundation of pathological anatomy, they are distinguished by a
universal historical and literary knowledge, by an all-encompassing
comprehension and control of the substance, by the thoroughness and
clarity of the representation. (1, p. 973).

What follows is a description of his character, as formulated by Kussmual:
Seeing the young clinician in his hospital was a useful thing and a
pleasure at the same time. For him, the activity there was not duty and
work, but pleasure and enjoyment; the clinic was not merely a
scientific workshop, but also a matter of the heart. You could not be
gentler, more humane with the sick, than Friedreich, his mild, quiet
dignity and safe action brought comfort and confidence to all, and for
some it was a cure. In the technique of physical examination, there was
no greater master. No one came close to him in the art of percussion.
One could find no better percussion hammers or plethimeters than
Friedreich's fingers. Even on the most corpulent individual, he lured
the notes far and wide. (2, pp. 203-204).

Friedreich reported initially in his chapter "Die Krankheiten des Herzens" ("The Diseases of the Heart") in Virchow's Handbuch der speciellen Pathologie und Therapie (Virchow's Handbook of Special Pathology and Therapy) in 1861, a "peculiar phenomenon of the cervical veins which he interpreted as a new sign for the diagnosis of cardiac adhesions (4)." In his paper titled "Zur Diagnose der Herzbeutelverwachsungen" ("For the Diagnosis of Pericardial Adhesions") published in 1864, Friedreich stated:
Since then not only the case to which I referred at that time attained
at necropsy, but also a second case has been found in my observation,
in which, in the presence of the same symptoms, the diagnosis of
pericardial obliteration was confirmed during life in the case of the
same subject, so that I can now consider the previous only with
probability-pronounced sentences as sufficiently well founded, and
believe [that I] can attach a new and essential sign to the still
somewhat uncertain diagnosis of the pericardial adhesions. At the same
time, the two cases to be described appear to me to be suitable for
rectifying and modifying some other points concerning the diagnosis of
pericardial adhesions. (5, pp. 296-297).
[T]he two cases presented here, which in many respects agree with each
other, seem so instructive in the diagnosis of pericardial dilatation
that their more specific communication, as well as a closer examination
of the phenomena observed during the course of the disease, may well be
justified. (5, p. 304).

He explained and proposed a pathogenesis for the occurrence of systolic retraction and diastolic recoil of the chest and later its effects on the jugular vein reasoning in both cases:
There seems to me to be no doubt that such widespread systolic
retraction must occur particularly when the heart shortens in the
longitudinal axis when the systole pulls the diaphragm strongly
upwards, and thus the points of insertion of the diaphragm on the
chest, inward, whose motion also increases the adjacent higher portions
of the thoracic wall, which are obliged to follow to a certain extent.
After all, the occurrence of this phenomenon seems to be much favored
by the more intimate adhesions of the lower surface of the heart with
the diaphragm, which existed in an unusually strong manner, especially
in the second case I have described. It seems probable to me that the
latter phenomenon occurs only in cases with such fixed adhesions to the
diaphragm, even without the obliteration of the remainder of the
pericardial cavity. Thus, this prevents the downward sliding motion of
the heart on the diaphragm, causing the diaphragm to be pulled upward
by the systolic shortening of the heart. In contrast, if there are no
diaphragmatic adhesions, despite existing pericardial adhesions in the
upper parts of the heart, the above phenomenon may well be missed by
freeing up the space caused by systolic shortening and elevation of the
heart either by the expansion of the lung or even by a slight upward
movement of the diaphragm. As a result of the pressure of the
intestinal gases, the shortening of the apex of the heart could at most
be marked by a systolic, circumscribed depression in the intercostal
space in question. The remarkable fact that the systolic retractions of
the chest wall were particularly pronounced at the level of the
inspiratory movements may also be used to support the view presented,
as the tighter, flattened, and shortened diaphragm had to be pushed
higher, especially with deep inspirations, and the visual effect is
more noticeable than during the flaccid and curved expiratory position
of the diaphragm (...) Apart from the diaphragmatic adhesions, a second
moment seems to require extensive systolic retraction of the chest
wall, namely, an unbroken and sufficiently strong energy of the cardiac
contractions, which has the task of overcoming the elasticity of the
thorax, which certainly provides a considerable resistance. (5, pp.

Friedreich described the appearance of the jugular veins during systole and diastole:
Simultaneously, with the diastolic recoil of the chest wall, a very
clearly visible, sudden, swelling, alternating with the carotid pulse,
followed by a rapid and brief jerking diastolic venous collapse could
be seen, and in one of the cases involved the entire supra-clavicular
region which in both the right and left side was recessed and pulled
inwards with a quick, short movement. In both cases, this diastolic
collapse was best seen in one of the right infraclavicular regions from
the bottom to the top, and extending downwards just below the clavicle
and externally at the greater skin-vein, especially recognized at the
anterior jugular vein. During the systolic retraction of the thoracic
wall, the veins were again gradually lifted and filled to a not
insignificant degree (in the second case with a double motion,
corresponding to the contraction of the atrium and ventricle), and at
the moment of diastole to collapse again to complete disappearances.
These described phenomena of the veins were so peculiar and striking
that they could not be confused with any of the more common occurrences
of the jugular veins. Evidently the emptying of the veins at the moment
of ventricular diastole must have been favored to a very special
degree, and it could be understood very well from the prevailing
circumstances. (5, pp. 310-311; emphasis added).

Furthermore, he accounted for the occurrence of this finding in adhesive pericarditis:
To a certain extent the sudden decreased pressure in the lungs produced
by the inward movement of the chest wall may be conducive to a rapid
outflow of blood from the jugular veins. This may well be compared to
the rapid diastolic recoil of the chest wall and retarding influences
of the previous systolic retraction to have a similar effect, with such
a rapid and deeper inspiratory movement, in the jugular veins.
Moreover, the reason for the above appearance seemed to be attributed
to a change of position of the diaphragm caused by the recoil of the
chest wall. As the result of the return of the ribs and the lower part
of the sternum into a deeper and flatter position, it was necessary for
the heart, which had adhered to the diaphragm, to undergo a movement
during diastole, contrary to the conditions prevailing under normal
conditions. (5, p. 311).

He acknowledged work by other authors in this field of study:
The phenomenon described here of a rapid diastolic collapse of the
cervical veins swelling gradually in systole has already been mentioned
by other observers, and Skoda regards this rare symptom as a sign of
paralysis of the right atrium, though it is difficult to see how it
should arise in the latter state. As a sign for pericardial
obliteration, however, I find the phenomenon not described or listed by
any of the authors known to me. (5, p. 312).

Thus, the Friedreich sign refers to diastolic collapse of the cervical veins in patients with adherent pericardium (Table 1). In a study of 15 cases of constrictive pericarditis and 17 normal controls, diastolic venous collapse was identified in 8 of 15 cases (6). Lang et al. identified the Friedreich sign in 15 of 16 patients with constrictive pericarditis. It is generally absent in cases of cardiac tamponade as it is more often associated with a restrictive and heavily calcified pericardial disease (7).

Duchenne Sign

Guillaume-Benjamin-Amand Duchenne (1806-1875) was born at Boulogne-sur-Mer (Boulogne), France, studied medicine in Paris where he was taught by eminent physicians such as Cruveilhier, Velpeau, Dupuytren, and Laennec, and graduated in 1831 (8, 9). Subsequently, he practiced in Boulogne, returning to Paris as a private practitioner in 1842 where he worked in Pierre-Francois Olive Rayer, Armand Trousseau, and Jean-Martin Charcot at Charite, Hotel-Dieu, and Salpetriere hospitals, respectively (8, 9). Both Trousseau and Charcot were influential in that they encouraged Duchenne to publish his discoveries (8). Despite not having an appointment or position at the University, he remained committed to clinical neurology research. He described his position related to this matter in his book titled De l'electrisation localisee et de son application a la pathologie et a la therapeutique (From Localized Electrization and Its Application to Pathology and Therapeutics) in response to criticism he received related to his failure to address the study of pathological anatomy during his clinical studies of glos-so-labial-laryngeal paralysis:
I must answer these reproaches that I do not think I have deserved.
Those who made it to me probably did not know that I was only allowed
to glean, so to speak, from our hospitals, and that if I have been able
to exist scientifically, it was because I have been fortunate enough to
collect, having browsed through the many services of hospital, the
clinical facts, which have been, I will not say disdainful, but which
had escaped the observation of all. Those who criticized me should have
known that when I discovered a morbid species not yet described, I was
not allowed to discuss subjects that I had made during my lifetime
clinical research. I would have had, it is true, the freedom to
complete these by anato-mo-pathological research, if I had been a
hospital doctor. But then, I could not have fulfilled the task of
researcher that I had imposed on myself, and I am convinced that my
principal work (among other things, progressive musculo-atrophy,
atrophic paralysis of childhood, progressive locomotor ataxia,
glosso-labio-laryngeal paralysis and pseudo-hyper-trophic paralysis)
would never have seen the light of day. To accomplish them, I needed a
wider field of observation, spanning all the hospitals in Paris. If,
therefore, I have renounced, and still renounce, the honors of an
official positions, it is because of my duty to give myself entirely
and freely to my irresistible taste for physiological and pathological
research. Should I be a subject of reproach for the disinterestedness
of having made science solely out of love for it? (10, p. 601).

Duchenne noted that there are different causes of diaphragmatic paralysis including the one caused by "palsies due to the inflammation of neighbouring organs" (11, p. 329). He further described the symptoms that occur in these conditions are
[n]oticeable during respiration, and are as follows: At the moment of
inspiration the epigastric and hypochondriac regions are depressed
although the chest dilates; during expiration these movements are
reversed. When the diaphragm is merely weak these signs are seen only
during forced respiration, but during tranquil breathing the bulging of
the belly and the expansion of the chest, and vice versa, occur
together, as in health. (11, p. 330; emphasis added).

Thus, the Duchenne sign refers to the presence of depression of the epigastrium and hypochondriac regions in patients with diaphragmatic paralysis and occasionally in pericardial effusion, although we were unable to confirm that he described the latter specifically in relation to pericardial effusion (12) (Table 1). Duchenne made numerous discoveries and contributions to the medical literature with eponymous conditions and diseases that bear his namesake, including the Duchenne attitude, Duchenne disease (Tabes dorsalis, progressive bulbar palsy), Duchenne paralysis, Duchenne--Aran disease, Duchenne Erb--Palsy paralysis, and Duchenne--Griesinger disease (Duchenne muscular atrophy or dystrophy) (8,13). We are unaware of any studies that evaluated the sensitivity or specificity of this sign.

Broadbent Sign

William Henry Broadbent (1835-1907) was born at Longwood, near Huddersfield, England, passed the qualifying examination in 1857 from the College of Physicians, London, and received his medical degree from the University of London in 1860 (14, 15). He served at St. Mary's Hospital in 1858, London Fever Hospital in 1860, and Western General Dispensary, as an outpatient, full, and later as a consulting physician (16). He was a member of the Royal College of Physicians in 1861, fellow in 1869, censor 1888-1890, and senior censor 1895-1896 (15, 17). He was appointed President of the Harveian Society in 1863, Medical Society of London in 1881, Clinical Society from 1887 to 1888, and Neurological Society from 1895 to 1896 (16, 17). In 1897, he was elected fellow of the Royal Society and received the honorary titles of LLD from the Universities of Edinburgh in 1896, St. Andrew in 1897, Toronto in 1906 and D.Sc. from the University of Leed in 1904 (15, 17-19). He is the recipient of a number of distinguished honors, including the Knight Commander of the Victorian Order in 1901, Grand Cross and Insignia of the Legion of Honour in 1904, and physician extraordinary to Queen Victoria and physician-in-ordinary to King Edward (15, 17, 18). His work spans primarily the fields of cardiology and neurology and additionally in the areas of cancer and typhoid (19).

In tribute to Broadbent's character, a former student wrote in an obituary the following description:
Those who kept in touch with him could always be sure of kindly and
wise counsel for the asking, whether the matter were one as to a
career, a perplexing case, or personal or domestic illness. In the
first two of these contingencies I have myself repeatedly experienced
his unfailing kindness; in the last I have known of instances where all
the engagements of a busy life have been put aside to make time to give
freely his aid in consultation at the bedside of some former pupil, not
only in or near London, but at distances involving a railway journey of
many hours each day. (17, p. 71).

William Broadbent described in 1895 in his paper titled "An Unpublished Physical Sign" the finding identified in four patients of a
[v]isible retraction, synchronous with the cardiac systole, of the left
back in the region of the eleventh and twelfth ribs, and in three of
which there is also systolic retraction of less degree in the same
region of the right back. In all the cases there is a definite history
of pericarditis, and in three of them there are other conditions
strongly suggesting an adherent pericardium. (20, p. 200; emphasis

Furthermore, he discussed the findings of adherent pericardium at the Medical Society's Transaction in 1898:
A systolic tug of the left false ribs posteriorly communicated by the
diaphragm may be conspicuous. The recoil from the drag may be so
distinct as to look and feel to the hand like pulsation, and in the
first case in which I observed it, now more than 20 years since-a case
of left empyema-it was taken for pulsation, and it was supposed that a
pulsating tumour of some kind underlay the empyema. A post-mortem
examination showed that the cause was adherent pericardium. (21, p. 25;
emphasis added).

He accounted for the proposed pathogenesis of this occurrence due to the
[d]iaphragm, which, if pulled upon, would have more effect on the
floating eleventh and twelfth ribs than on the other more fixed ones.
In cases of large heart with adherent pericardium there is a
considerable area of the ventricles closely adherent to the central
tendon of the diaphragm, and the powerful contraction of the
hypertrophied heart must give a decided tug to this structure. That it
should affect the ribs more often on the left side would be expected
from the adhesion being mainly to the left of the middle line; the
liver also, which is often large in these cases, may restrain the
movement to the right. (22, p. 200).

He believed that "systolic retraction of the lower ribs on the lateral or posterior aspect of the thorax is of the greatest importance, and can scarcely be due to anything else than pericardial disease" (22, p. 56; emphasis added). Broadbent sign thus refers to the systolic retraction of the chest wall near the eleventh and twelfth rib posteriorly due to pericardial adhesions (Table 1). We are unaware of any study that evaluated the sensitivity or specificity of this sign.


From 1864 to 1895, physicians continued to observe signs related to protrusion and retraction of the chest wall during cardiac contraction and respiration. Friedreich's observation is notable as it provided insights of events occurring in the jugular veins that correlate with the cardiac cycle. An appreciation of these signs is important as it assists clinicians to understand the pathophysiologic mechanism of pericardial disease.

Peer-review: Externally peer-reviewed.

Author Contributions: Conceived and designed the experiments or case: FY, HT, ESY, JJM, SY. Performed the experiments or case: Not applicable. Analyzed the data: FY, HT, ESY, JJM, SY. Wrote the paper: FY, HT, ESY, JJM, SY.

Conflict of Interest: The authors have no conflict of interest to declare.

Financial Disclosure: The authors declared that this study has received no financial support.


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(2.) Kussmaul A. Nikolaus Friedreich. Deutsches Arch f Klin Med 1883;32:191-208.

(3.) Miller JW. Friedreich's Ataxia. Medical Reviews of Reviews 1916;22:192-5.

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(18.) Obituary Note. Sir William Broadbent Bart. St. Louis Med Rev 1907;56: 71-72 18. Sir William Henry Broadbent, Bart; K.C.V.O; 1835-1907. vii-x. (cited 2018 December 15) Available from:

(19.) William Henry (Sir) Broadbent. Lives of the fellows. Royal College of Physicians. Available at: URL:

(20.) Broadbent W. An unpublished physical sign. Lancet 1895;2:200-1.

(21.) Broadbent W. Adherent Pericardium. In: Selections from the Writings, Medical and Neurological of Sir William Broadbent, Bart; K.C.V.O. London: Henry Frowde Oxford University Press; 1908, pp. 21-26.

(22.) Broadbent JFH. Adherent Pericardium. New York: William Wood & Company; 1896.

Fan Ye (1) [iD], Halil Tekiner (2)[iD], Eileen S Yale (3)[iD], Joseph J Mazza (4)[iD], Steven Yale (5)[iD]

(1) Graduate Medical Education, University of Central Florida College of Medicine Orlando, FL, USA (2) Department of the History of Pharmacy and Ethics, Erciyes University School of Pharmacy, Kayseri, Turkey (3) Department of General Internal Medicine, University of Florida, Gainesville, FL, USA (4) Marshfield Clinic Research Institute, Marshfield, WI, USA (5) Department of Internal Medicine, University of Central Florida College of Medicine, Orlando, FL, USA





Available Online Date



Steven Yale, University of Central Florida College of Medicine 6850 Lake Nona Blvd, Orlando, FL 32827, USA

Phone: (407) 266-1000


Cite this article as: Ye F, Tekiner H, Yale ES, Mazza JJ, Yale S. Physical Signs of Inspection and Medical Eponyms of Pericarditis Part II: 1864 to 1895. Erciyes Med J 2019; 41(2): 230-4.

DOI: 10.14744/etd.2019.37659
Table 1. Inspection and pericardial eponyms signs from 1864 to 1895

Name        Year   Description of sign             Significance

Friedreich  1864   During diastole, there is a     Adhesive pericarditis
                   rapid and brief jerking and
                   venous collapse seen best
                   at the anterior jugular
                   vein. During systole,
                   the veins become gradually
                   lifted and filled.
Duchenne    1883   During inspiration, the         Pericardial effusion
                   epigastric and hypochondriac
                   regions are depressed, and
                   the chest dilates.
                   During expiration, these
                   movements are reversed. When
                   the diaphragm is weak, these
                   signs are seen only during
                   forced respiration.
Broadbent   1895   Retraction synchronous with     Adherent pericardium
                   the cardiac systole occurring
                   posteriorly in the region
                   of the left and right
                   eleventh and twelfthribs.
                   This is most marked on the
                   left compared to the right
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Author:Ye, Fan; Tekiner, Halil; Yale, Eileen S.; Mazza, Joseph J.; Yale, Steven
Publication:Erciyes Medical Journal
Article Type:Report
Date:Jun 1, 2019
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